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I note the How To Treat A Hypo information. As a T1D for 58 years I have a 'passing familiarity' with hypos. What concerns me is that:
a) whilst glucose is listed as the first option for treatment, the next options are 'fizzy drinks, sweets and fruit juice'.
From past clinical experience and my diabetes education, these later options contain sucrose,(table sugar) which the saliva in our mouth
usually breaks down to glucose and fructose (fruit sugar). The glucose is needed to raise our BGLs but the fructose does not of itself raise
blood glucose levels. Fruit juices also contain levels of fructose and over many years the cultivation of fruit has led to higher levels in fruit.
What is worse, such rapidly absorbed fructose is coped with by liver the same way alcohol is - by being turned into fat, and stored in the liver.
Fructose is sometimes referred to as children's alcohol, you get the liver problems like fatty liver , just not with alcohol itself.
You might ask, but what does it matter having sucrose as a hypo remedy on one occasion?
But, how many hypos can happen in a day, a week or a month? - with T1D as a child like I was - how many typos and treatments over years?
Fortunately for me now on a very low carb diet, hypos are rare and mild, and I have routinely used glucose for hypos except on the very rare
occasion where I have run out, it got wet and dissolved etc. Then any glucose such as in the other portions mentioned above is a last resort.
But, as Dr Bernstein states (paraphrased), 'the most usual cause of hypoglycaemia is from high carb diets requiring industrial doses of insulin'
b) If I suffer a rebound high BGL from treating a hypo, or a high BGL for any reason above 7 mmol/l, this leads to a biochemical sequence called the
POYOL pathway - whereby 30% of that BGL is converted to fructose whereas under 7 mmol/l the amount of BGL converted to fructose is only 3 to 5%.
What can fructose from a) or b) do beyond the developing of fatty liver - the other complications associated with repeated exposure to fructose
include damage to the back of the eyer (retina), cataracts in the lenses of the eye, damage to kidneys and nerves.
If you think that a BGL of 7 mmol/l just comes and goes, there is a equivalence chart of average BGL vs HBA1c - two derivations 1) from the Diabetes
Control and Complications Trial (DCCT) and another made up by a committee of the ADA and commercial interest titled the ADAG. see diagram.
An average BGL of 7 mmol/l = 5.7% (DCCT) or about 6% (ADAG). Please think about that the next time you see the official recommnedatons for HBA1c !!
/Users/tonysangster/Desktop/IMG_2500.jpeg
a) whilst glucose is listed as the first option for treatment, the next options are 'fizzy drinks, sweets and fruit juice'.
From past clinical experience and my diabetes education, these later options contain sucrose,(table sugar) which the saliva in our mouth
usually breaks down to glucose and fructose (fruit sugar). The glucose is needed to raise our BGLs but the fructose does not of itself raise
blood glucose levels. Fruit juices also contain levels of fructose and over many years the cultivation of fruit has led to higher levels in fruit.
What is worse, such rapidly absorbed fructose is coped with by liver the same way alcohol is - by being turned into fat, and stored in the liver.
Fructose is sometimes referred to as children's alcohol, you get the liver problems like fatty liver , just not with alcohol itself.
You might ask, but what does it matter having sucrose as a hypo remedy on one occasion?
But, how many hypos can happen in a day, a week or a month? - with T1D as a child like I was - how many typos and treatments over years?
Fortunately for me now on a very low carb diet, hypos are rare and mild, and I have routinely used glucose for hypos except on the very rare
occasion where I have run out, it got wet and dissolved etc. Then any glucose such as in the other portions mentioned above is a last resort.
But, as Dr Bernstein states (paraphrased), 'the most usual cause of hypoglycaemia is from high carb diets requiring industrial doses of insulin'
b) If I suffer a rebound high BGL from treating a hypo, or a high BGL for any reason above 7 mmol/l, this leads to a biochemical sequence called the
POYOL pathway - whereby 30% of that BGL is converted to fructose whereas under 7 mmol/l the amount of BGL converted to fructose is only 3 to 5%.
What can fructose from a) or b) do beyond the developing of fatty liver - the other complications associated with repeated exposure to fructose
include damage to the back of the eyer (retina), cataracts in the lenses of the eye, damage to kidneys and nerves.
If you think that a BGL of 7 mmol/l just comes and goes, there is a equivalence chart of average BGL vs HBA1c - two derivations 1) from the Diabetes
Control and Complications Trial (DCCT) and another made up by a committee of the ADA and commercial interest titled the ADAG. see diagram.
An average BGL of 7 mmol/l = 5.7% (DCCT) or about 6% (ADAG). Please think about that the next time you see the official recommnedatons for HBA1c !!
/Users/tonysangster/Desktop/IMG_2500.jpeg
